Body water is divided into cellular and extracellular compartments. Drinking behavior can be induced by a selective reduction of either of these two compartments. The renal renin-angiotensin system has been implicated as a hormonal mediator of thirst which is activated by manipulations which produce a reduced extracellular volume. In order to achieve a full understanding of how the renin- angiotensin system mobilizes drinking behavior it is critical that we understand how these agents interact with the brain. Experimental evidence provides some support for a hypothesis of ventricular access of angiotensin to a periventricular receptor site sensitive to angiotensin per se be positively identified in the cerebrospinal fluid in order to support the idea of ventricular access. The radioimmunoassay of cerebrospinal fluid following infusions of dipsogenic doses of angiotensin promises to provide a means for determining if angiotensin enters the ventricular system. If it is demonstrated that exogenous, systemically infused angiotensin does have ready access to the cerebrospinal fluid then it becomes important to investigate whether the ventricular mechanism is involved when the endogenous renin-angiotensin system is activated. By applying various experimental manipulations which elicit thirst and then examining the cerebrospinal fluid for changes in angiotensin levels, the importance of angiotensin access to the ventricular system and drinking behavior can be further assessed. Finally, by examining the changes in cerebrospinal fluid angiotensin following treatment of nephrectomized animals treated with hyperoncotic colloid, it may be possible to implicate the newly discovered brain renin-angiotensin system as playing a significant role in drinking behavior.